ALK-positive plasmablastic B-cell lymphoma with expression of the NPM-ALK fusion transcript: report of 2 cases

Onciu, Mihaela; Behm, Frederick G.; Downing, James R.; Shurtleff, Sheila; Raimondi, Susana C.; Ma, Zhigui; Morris, Stephan W.; Kennedy, Wren; Jones, Sandra C.; Sandlund, John T.

doi:10.1182/blood-2003-04-1095

Cited by 141 publications

(124 citation statements)

References 12 publications

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“…15,16 Even the 'classical' t(2;5)(p23;q35) with NPM as the fusion partner driving ALK overexpression has been reported to occur in DLBCL with plasmablastic morphology. 17 However, our lymphoma case lacks evidence of an altered ALK gene configuration, and it remains to be determined if the presence of ALK is a mere accident rather than an oncogenic phenomenon in these translocation-negative cases, in a similar manner as has been demonstrated for neuroblastomas expressing full-length ALK. 40 HHV-8-associated plasmablastic lymphomas have also been described recently.…”

Section: Spectrum Of Plasmablastic Lymphomas In the Who Classificationmentioning

confidence: 53%

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Diffuse large B-cell lymphomas with plasmablastic/plasmacytoid features are associated with TP53 deletions and poor clinical outcome

et al. 2003

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Section: Spectrum Of Plasmablastic Lymphomas In the Who Classificationmentioning

confidence: 53%

“…15,16 Even the 'classical' translocation t(2;5)(p23;q35) involving the nucleophosmin (NPM) gene on chromosome 5q has been reported in two plasmablastic lymphomas. 17 Thus, the term 'plasmablastic' seems to encompass a wide and ever-growing spectrum of lymphomas with different clinical and biological features.…”

Section: Introductionmentioning

confidence: 99%

Diffuse large B-cell lymphomas with plasmablastic/plasmacytoid features are associated with TP53 deletions and poor clinical outcome

et al. 2003

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“…3,4 Diffuse large B-cell lymphoma with expression of ALK and extramedullary myeloid tumor can be excluded by immunohistochemical studies for ALK and myeloid markers, respectively. 5,6 However, in many cases of plasmablastic lymphoma, the most difficult issue in the differential diagnosis is excluding plasmablastic plasma cell myeloma with extramedullary involvement. This is a clinically important distinction, since plasmablastic lymphoma is listed in the WHO classification as a variant of diffuse large B-cell lymphoma implying that therapy for diffuse large B-cell lymphoma is appropriate, while plasma cell myeloma cases are treated with different chemotherapy regimens.…”

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confidence: 99%

Plasmablastic lymphomas and plasmablastic plasma cell myelomas have nearly identical immunophenotypic profiles

Vega

Chang

Medeiros³

et al. 2005

Modern Pathology

322

299

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Plasmablastic lymphoma is an aggressive neoplasm that shares many cytomorphologic and immunophenotypic features with plasmablastic plasma cell myeloma. However, plasmablastic lymphoma is listed in the World Health Organization (WHO) classification as a variant of diffuse large B-cell lymphoma. To characterize the relationship between plasmablastic lymphoma and plasmablastic plasma cell myeloma, we performed immunohistochemistry using a large panel of B-cell and plasma cell markers on nine cases of plasmablastic lymphoma and seven cases of plasmablastic plasma cell myeloma with and without HIV/AIDS. The expression profiles of the tumor suppressor genes p53, p16, and p27, and the presence of Epstein-Barr virus (EBV) and human herpes virus type 8 (HHV-8) were also analyzed. All cases of plasmablastic lymphoma and plasmablastic plasma cell myeloma were positive for MUM1/IRF4, CD138, and CD38, and negative for CD20, corresponding to a plasma cell immunophenotype. PAX-5 and BCL-6 were weakly positive in 2/9 and 1/5 plasmablastic lymphomas, and negative in all plasmablastic plasma cell myelomas. Three markers that are often aberrantly expressed in cases of plasma cell myelomas, CD56, CD4 and CD10, were positive in 5/9, 2/5, and 6/9 plasmablastic lymphomas, and in 3/7, 1/5, and 2/7 plasmablastic plasma cell myelomas. A high Ki-67 proliferation index, overexpression of p53, and loss of expression of p16 and p27 were present in both tumors. No evidence of HHV-8 infection was detected in either neoplasm. The only significant difference between plasmablastic lymphoma and plasma cell myeloma was the presence of EBV-encoded RNA, which was positive in all plasmablastic lymphoma cases tested and negative in all plasma cell myelomas. In conclusion, most cases of AIDS-related plasmablastic lymphoma have an immunophenotype and tumor suppressor gene expression profile virtually identical to plasmablastic plasma cell myeloma, and unlike diffuse large B-cell lymphoma. These results do not support the suggestion in the WHO classification that plasmablastic lymphoma is a variant of diffuse large B-cell lymphoma.

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“…11 Subsequently, ALK rearrangements were found in several phenotypically different hematologic neoplasms [12][13][14] and in histogenetically unrelated inflammatory myofibroblastic tumor. [15][16][17][18] Recently, ALK rearrangements and EML4-ALK and KIF5B-ALK fusions were discovered in a subset of non-small cell lung carcinomas; 19,20 proteomics reports suggested a possible TPM4-ALK fusion in esophageal carcinoma; 21,22 and an exon array profiling study demonstrated the EML4-ALK fusion in 2.5% of breast and colon cancers.…”

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confidence: 99%

Renal cell carcinoma with novel VCL–ALK fusion: new representative of ALK-associated tumor spectrum

et al. 2011

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Renal cell carcinoma represents a model for contemporary classification of solid tumors; however, unusual and unclassifiable cases exist and are not rare in children and young adults. The anaplastic lymphoma kinase (ALK) gene has recently been implicated in subsets of pulmonary, esophageal, breast, and colon cancers. These findings strengthen the importance of molecular classification of carcinomas across different organ sites, especially considering the evolving targeted anticancer therapies with ALK inhibitors. In the current study of six pediatric renal cell carcinomas, two cases exhibited structural karyotypic abnormalities involving the ALK locus on chromosomal band 2p23. Fluorescence in situ hybridization (FISH) studies were positive for an ALK rearrangement in one case, and subsequent 5 0 rapid amplification of cDNA ends analysis of this tumor revealed that the 3 0 portion of the ALK transcript encoding for the kinase domain was fused in frame to the 5 Keywords: ALK; FISH; fusion gene; renal cell carcinoma; translocation; VCL Renal cell carcinoma has an incidence of 209 000 cases per year and is responsible for 102 000 deaths worldwide annually. 1,2 Approximately 80% of all renal carcinoma cases are currently classified as clear cell, papillary, or chromophobe subtypes with discrete molecular abnormalities characteristic for each group. 2-7 Rare subtypes have also been defined by the 2004 World Health Organization classification and include collecting duct, multilocular cystic, mucinous tubular and spindle cell, medullary, and Xp11.2 translocation-and neuroblastoma-associated carcinomas; each of these subtypes constitutes B1% of all primary kidney epithelial tumors and the three latter subtypes are diagnosed predominantly in children. 8,9 Additional

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ALK-positive plasmablastic B-cell lymphoma with expression of the NPM-ALK fusion transcript: report of 2 cases

Cited by 141 publications

References 12 publications

Diffuse large B-cell lymphomas with plasmablastic/plasmacytoid features are associated with TP53 deletions and poor clinical outcome

Diffuse large B-cell lymphomas with plasmablastic/plasmacytoid features are associated with TP53 deletions and poor clinical outcome

Plasmablastic lymphomas and plasmablastic plasma cell myelomas have nearly identical immunophenotypic profiles

Renal cell carcinoma with novel VCL–ALK fusion: new representative of ALK-associated tumor spectrum

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